TLR4/NF-KB SIGNALING PATHWAY IS A KEY PATHOGENIC EVENT LEADING TO KIDNEY DAMAGE IN UUO INDUCED RENAL FIBROSIS | ||||
| Al-Azhar Journal of Pharmaceutical Sciences | ||||
| Article 5, Volume 61, Issue 1, March 2020, Page 61-76 PDF (1.29 MB) | ||||
| Document Type: Review Article | ||||
| DOI: 10.21608/ajps.2020.86015 | ||||
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| Author | ||||
| Amr Mabrouk Allam | ||||
| Depatment of Biochemistry, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, Assiut, Egypt | ||||
| Abstract | ||||
| Chronic Kidney Disease (CKD) is a public health problem worldwide. Renal fibrosis is regarded as the final common pathologic manifestation of a wide variety of CKDs. There are many molecules and cells that are associated with progression of renal fibrosis. The toll like receptor (TLR) family serves an important regulatory role in the innate immune system, and recent evidence has implicated TLR signaling in the pro inflammatory response of a variety of endogenous and exogenous stimuli within the kidney. Innate immune activation via TLR4 contributes to acute kidney injuries but its role in tissue remodeling during CKD is unclear. The current study aimed to determine the expression pattern of renalTLR4, nuclear factor kappa B (NF-kB) and alpha-smooth muscle actin (a-SMA) after 3, 7 and 14 days of unilateral ureter obstruction (UUO) model in mice, and explore the impact of TLR4 expression onobstruction-induced renal fibrosis and myofibroblast proliferation. We reported an elevated expression of TLR4 and its downstream modulator NF-kB in all grades of renal fibrosis of UUO mice. Significant increase in interstitial collagen deposition and myofibroblast activation (a-SMA) were also evident in UUO mice. In conclusion, our findings confirmed previous reports which identified TLR4/NF-kB signaling pathway as a significant mediator of both inflammatory and fibrotic renal injury. | ||||
| Keywords | ||||
| Toll like receptor; Nuclear factor kappa B; Inflammation; kidney; Unilateral ureteral obstruction; Alpha-smooth muscle actin; Fibrosis | ||||
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